By Z. Lukar. Mississippi Valley State University.

In contrast generic 250mg cefadroxil with amex, all other branches that arise anteriorly represent intraperitoneal arteries that supply the digestive system buy 250mg cefadroxil with amex, including the celiac artery (with its left gastric order cefadroxil 250mg amex, splenic, and hepatic branches) and the superior and inferior mesenteric arteries. Distally, the aorta bifurcates into the common iliac arteries and also gives rise to the middle sacral artery. Ductus Arteriosus During fetal life, the ductus arteriosus provides an avenue for communication between the pulmonary and systemic circulations. It is interposed between the proximal portion of the left pulmonary artery and the undersurface of the aortic arch; during intrauterine life, its diameter is similar to that of the descending thoracic aorta and is larger than that of the right or left pulmonary artery. Most of the right ventricular output bypasses the lungs and enters the aorta via the ductus arteriosus. However, soon after birth and with expansion of the lungs, the ductus functionally closes, pulmonary vasodilation occurs, and the entire right cardiac output passes through the lungs (see Chapters 28 and 31). Throughout gestation, structural changes take place that prepare the ductus arteriosus for rapid functional closure soon after birth (24). Initially, this vessel has the appearance of a muscular artery, in contrast to the elastic arteries to which it connects. During the third trimester, proliferative fibroelastic intimal cushions become prominent and medial thickening results from smooth muscle proliferation and the deposition of collagen, elastin, and glycoproteins. Ultrastructurally, medial smooth muscle cells change from the secretory to the contractile type. Blurring of intimal–medial junctions, coupled with haphazard arrangement of muscle bundles, produces an appearance similar to that of fibromuscular dysplasia. Adventitial elastic fibers become prominent, particularly at each end of the artery. Ductal vasoconstriction, over the next several weeks, is accompanied by focal medial necrosis, medial edema, disruption of the internal elastic lamina, and mural thrombosis. Subsequently, the deposition of elastin within the arterial wall becomes marked and focal areas of calcification are the rule, resulting in complete and permanent closure of the ductus arteriosus, persisting from then on as the ligamentum arteriosum. Not surprisingly, ductal closure is hampered in both infants born at high altitude where oxygen tension is lower and in those born prematurely. Both genetic factors and prenatal infection may also play a role in patients with ductus arteriosus patency. In general, closure of the ductus arteriosus begins near the pulmonary artery and progresses toward the aorta. If this process is incomplete, a small ductal diverticulum remains that characteristically emanates from the undersurface of the aortic arch. Rarely, ductal aneurysms, dissections, or ruptures occur and may be associated with underlying connective tissue disease, surgical manipulation, or active/healed arteritis. Their ostia (ostiums) are circular to elliptical and originate midway between the aortic valve commissures and about two-thirds of the distance between the annulus and the sinotubular junction. The right coronary artery originates nearly perpendicularly from the right aortic sinus. In contrast, the left main coronary artery arises at an acute downward angle and travels parallel to its aortic sinus wall. The major epicardial arteries include the left main, left anterior descending, circumflex, and right coronary arteries. Branches of the left anterior descending artery are called diagonals, whereas branches of the right and circumflex arteries are called marginals (Fig. Septal perforators represent long intramural branches of the anterior and posterior descending arteries that supply the ventricular septum; hence, are not epicardial branches. Proximally, the right coronary artery travels between the main pulmonary artery and the right atrium and is covered by the right atrial appendage. In about 60% of subjects, the first branch is the conus coronary artery, which supplies the right ventricular outflow tract; in the other 40%, this artery arises independently from the right aortic sinus (25). Marginal branches include several small vessels and a prominent acute marginal artery. Beyond the acute margin, along the inferior surface of the heart, the length of the right coronary artery varies inversely with that of the circumflex artery. The left main coronary artery lies between the main pulmonary artery and the left atrium and is covered by the left atrial appendage. It bifurcates into left anterior descending and circumflex branches in most individuals but trifurcates in some, with an intermediate artery emanating between the other two vessels. A short (<8 mm) left main artery is often associated with left coronary dominance. The vast majority of left coronary artery blood flow takes place during ventricular diastole. Traveling within the anterior interventricular groove, the left anterior descending artery wraps around the apex and extends for a variable distance in the posterior interventricular groove. Including its diagonal and septal perforating branches, this vessel supplies the anteroseptal and anterolateral walls, part of the anterolateral mitral papillary muscle, and the entire apex of the left ventricle. Bridges of myocardium cover small lengths of the left anterior descending artery in about 10% of human hearts, but usually do not interfere with diastolic myocardial perfusion (26). It generally terminates just beyond its obtuse marginal branches and nourishes the lateral wall of the left ventricle and part of the anterolateral mitral papillary muscle. About 20% of human hearts exhibit shared coronary dominance, such that both the right and circumflex arteries provide posterior descending branches. A: The right and circumflex arteries travel in the atrioventricular groove, near the tricuspid and mitral valves, respectively (cardiac base). B: The anterior and posterior descending arteries travel in the interventricular groove and demarcate the plane of the ventricular septum (superior and inferior views). C: Coronary dominance is determined by the origin of the posterior descending branch. D: The anterior cardiac veins empty directly into the right atrium, whereas the other major epicardial veins drain into the coronary sinus. Nourishment for the right and left bundle branches is provided by other septal perforator branches of the anterior and posterior descending arteries. Similarly, the anterior and posterior descending coronary arteries course within the interventricular grooves and indicate the plane of the ventricular septum. Consequently, for surgeons and pathologists, the epicardial coronary arteries are reliable external landmarks for determining relative chamber sizes and valve locations. Coronary Veins The coronary veins and cardiac lymphatics work in concert to remove excess fluid from the myocardial interstitium and the pericardial sac. The venous circulation of the heart consists of a coronary sinus system, an anterior cardiac venous system, and a thebesian venous system (Fig. The great cardiac vein travels beside the left anterior descending and circumflex coronary arteries to merge with the coronary sinus. The coronary sinus, in turn, receives the left-posterior, middle, and small cardiac veins, as well as several smaller tributaries, before joining the right atrium.

Recently purchase cefadroxil on line amex, new assays have been introduced to offer an assessment of platelets for aspirin and clopi- dogrel (Plavix) resistance safe cefadroxil 250 mg. Platelet aggregation is now performed not only to assess baseline platelet function but also to determine if an antiplatelet medication has produced the desired platelet inhibition buy cheap cefadroxil 250 mg on line. In this situation, a desired response is often poor platelet function because it implies that the antiplatelet medication is effective. In addition, a number of aspirin preparations have names that do not suggest that the pill or cap- sule is indeed aspirin. Because of this, patients can inadvertently ingest aspirin and report no aspirin ingestion. In this situation, platelet dysfunction will be observed as a result of the antiplatelet medica- tion and obscure any endogenous abnormalities that might be present and detectable. If aspirin has been avoided for fve to seven days, most of the decreased platelet function should be restored. If aspirin has been avoided for 10 to 14 days, in the absence of other variables, platelet function should be fully restored. Recent ingestion of clopidogrel will also result in abnormal platelet function if the patient effectively converts the oral prodrug into the active antiplatelet medication. Platelet function returns to normal approximately seven days after the last dose of clopidogrel. This test is associated with many variables, and currently, it is rarely used to assess the adequacy of platelet function. In particular, it has been shown to be a poorly predictive test for platelet function in the patient anticipating surgery. In a stand- ard platelet-rich plasma–based platelet aggregation study, for example, the clinical signifcance of a mildly decreased response to epinephrine is highly uncertain. Minor abnormalities may or may not be associated with an increased risk for bleeding. If possible, repeat testing for platelet function in the absence of a drug suspected to be responsible for platelet dysfunction is likely to be informative. Technical variables that can produce false results (positive or negative) include the following: allow- ing the sample of platelet-rich plasma to sit too long before a platelet agonist is added; cooling the platelet-rich plasma before the addition of the platelet agonist; addition of the platelet agonist to the wall of the tube containing platelet-rich plasma in such a way that the agonist never fully mixes with the platelet suspension; contamination of the platelet-rich plasma with red blood cells that do not clump in the presence of the platelet agonist and obscure the platelet response; and not assessing the activity of platelet agonists with normal donor platelets as controls when the platelet aggregation responses of the patient are reduced. This cytochrome system metabolizes clopidogrel from an oral pro- drug to an active platelet antagonist. A particularly signifcant controversy relates to the concept of aspirin sensitivity testing. The lack of a con- sensus-driven guideline for aspirin resistance testing is explained by several factors. It is impossible to know which test result refects the true response of the platelets to aspirin in vivo. A second factor is that there is no universally accepted defnition of aspirin resistance. A third issue is that apparent aspirin resistance in many patients taking 81 mg of aspirin daily is overcome by simply increas- ing the dose to 325 mg daily. There is one circumstance that has been widely accepted to produce aspirin resistance. It has been shown that ingestion of a nonsteroidal anti-infammatory drug, such as ibuprofen, shortly preceding aspirin ingestion can prevent the permanent antiplatelet effect induced by aspirin. Platelets can recover ade- quate function after exposure to a nonsteroidal anti- infammatory drug, usually within 24 hours after the drug has been taken. Therefore, aspirin-treated platelets that have been previously exposed to a nonsteroidal anti-infammatory drug are commonly found to be aspirin resistant because they recover platelet function after exposure to aspirin. Delta checks should be used in the labo- ratory to identify potential patient identifcation errors. The blood should be well mixed after collection into the tube to prevent clot formation and transported to the laboratory in a timely fashion. They should be rejected if there are visible clots or if there is discernible hemolysis or lipemia. Smears that are too thick, poorly smeared, or air dried can have red cell artifacts. For example, schistocytes should have sharp edges and angles with no central pallor, and target cells and echinocytes should be widely distributed on the smears rather than concentrated on a single part of the smear. The dif- ferential diagnosis of microcytic anemia includes iron defciency, anemia of chronic disease, and selected hemoglobinopathies, including thalassemia. Distinguishing the causes of microcytic anemia can be complicated when there are two or more different disorders at the same time, often leading to incorrect diagnoses. Although ferritin is the most sensitive indicator of iron defciency, one should not rely on ferritin alone, as it can be falsely elevated in infammatory states. RetHe should be reviewed when it is diffcult to distinguish between iron defciency and anemia of chronic disease. This is especially important in immigrants from areas with a high inci- dence of hemoglobin mutations who may not have received newborn screening for these disorders. The number of circulating reticulocytes is indicative of underlying erythropoiesis; that is, when erythropoiesis is stimulated, the number of circulating reticulocytes increases. These fndings may be accompa- nied by a “left shift,” an increase in circulating neutro- phil precursors, such as bands and metamyelocytes. These fndings are a common reactive response to bacterial infections and physiologic stress. Similarly, eosinophilia can be caused be parasitic infections or allergic reactions. However, similar fndings are seen in neoplastic disorders, such as chronic myelogenous leukemia (Cml) or eosinophilic leukemia. Particular attention should be paid to the distribution of immature cells and the presence of increased atypical basophils and blasts. These may include anemia, throm- bocytopenia or marked thrombocytosis, and baso- philia, which could point to neoplastic disorders. Reactive lymphocytosis is often accompanied by a variety of changes in lymphocyte morphology. Particular care should be taken in young children, in whom normal immature lymphocytes may circulate. These conditions should be ruled out by a careful clinical history, physical examination, and appropriate laboratory testing prior to a diagnosis of or referral for leukemia or lymphoma. This leads to cytopenia-associated complications, including susceptibility to infection, anemia, and bleeding diath- esis. Additionally, there is increased risk for the devel- opment of acute myeloid leukemia.

A technique has been described that allows quantitative assessment of abnormalities in a pulmonary wedge angiogram (12) cheap 250 mg cefadroxil with amex. A balloon catheter is directed to the origin of the axial artery of the posterior basal segment of the right lower lobe buy cheap cefadroxil 250 mg on-line; contrast material is injected buy cefadroxil with a visa, and the injection is filmed on biplane cineangiography. The rate of tapering of the arteries is assessed by measuring the length of a segment over which the lumen diameter narrows from 2. More abrupt arterial tapering is suggestive of more severe changes in the intra- acinar arteries, assessed both morphometrically and by the Heath–Edwards classification (Table 65. Quantitative structural analysis of the pulmonary vascular bed in congenital heart defects. Pulmonary stenosis or previous placement of a pulmonary artery band, owing to poststenotic dilation, will give the impression of rapid tapering. With advanced vascular disease, there is sometimes such extensive intimal hyperplasia that the vessel appears narrowed all the way from the hilum so that abrupt tapering is no longer apparent. In this situation, however, the background haze is absent and the pulmonary circulation time is usually prolonged. If the injection of contrast fails to fill the vessels all the way out to the pleura, the background will appear dark, and if the balloon does not completely occlude the vessel, the false impression of a dense background will be created owing to filling of capillaries and veins. Assessment of the circulation time depends on the exclusion of pulmonary vein stenosis and intrapulmonary shunting. Intravascular ultrasound could be investigated to estimate the severity of pulmonary vascular disease at least in proximal vessels. Optical coherence tomography is a new technique that can resolve neointimal lesions in very small arteries and may hold greater promise, but has just recently been applied clinically to assess coronary stent stenosis (13). Early studies of optical coherence tomography in the pulmonary vasculature studies have shown correlation in pulmonary artery remodeling with changes in histology (14). Reactive Pulmonary Circulation A major challenge in pediatric cardiology is to understand and control the reactive pulmonary circulation, which can be particularly problematic in the early postoperative period. The pulmonary hypertensive crisis, as it has been called, is thought to result from interaction of a hypertrophied and perhaps hypercontractile circulation with an injured vascular endothelium, with platelets and leukocytes that were exposed to postcardiopulmonary bypass and hypothermia and may more easily degranulate and release potent vasoconstrictor agents, particularly thromboxanes and leukotrienes. In recent studies, increased density of neuroepithelial bodies has been observed in the airways of patients at risk for this complication (15). The neuroendocrine cells, which are also oxygen sensors, contain bombesin and serotonin, agents known to be potent vasoconstrictors. There is also an increase in vasoconstrictor neuropeptide-containing nerves (16) (Fig. Because most of the pulmonary hypertensive crises occur while weaning from the ventilator, it is tempting to speculate that swings in airway pressure might lead to degranulation of the neuroepithelial cells and release of the vasoconstrictor substances. Moreover, there is a striking decrease in lung compliance accompanying the pulmonary hypertensive crisis. In ultrastructural lung biopsy studies from patients with congenital heart defects and pulmonary hypertension, alterations in endothelial cells support endothelial dysfunction as a cause of heightened pulmonary vascular reactivity and also relate endothelial dysfunction to the pathogenesis of progressive pulmonary vascular disease. On scanning electron microscopy, the endothelial surface of normal thin-walled pulmonary arteries has a “corduroy-like” appearance in that the cells form narrow, even ridges. In contrast, the endothelial surface of hypertensive thick-walled pulmonary arteries has a “cable-like” texture in that the cells form deep, twisted ridges. The hypertensive endothelium may be predisposed to interact abnormally with marginating blood elements, such as platelets and leukocytes. This might result in the release of pulmonary vasoconstrictor substances and smooth muscle mitogens (17). On transmission electron microscopy, the endothelium appeared to show heightened metabolic activity with an increased rough endoplasmic reticulum. The subendothelium of the muscular arteries is also abnormal in that there appears to be degradation and neosynthesis of the internal elastic lamina. This observation provided an important clue related to the discovery of heightened elastolytic activity in the vessel wall associated with the initiation and progression of pulmonary vascular disease. This could indeed account for the development of platelet fibrin microthrombi in the postoperative period and for abnormal release of vasoactive compounds causing increased vascular reactivity. B: Tyrosine hydroxylase immunoreactive perivascular nerve fibers at the advential–medial border of an alveolar duct artery in a child aged 2 1/2. A study of nerves containing peptides in the pulmonary vasculature of healthy infants and children and of those with pulmonary hypertension. There also is evidence that production of the vasoconstrictor endothelin also might be increased in patients with pulmonary hypertension and congenital heart defects (21). Many patients with high-flow congenital heart defects that are operated upon in a timely fashion show a fall in pulmonary artery pressure and return to normal resting hemodynamics, indicating resolution and regression of pulmonary hypertensive structural changes. This is supported by experimental studies and by anecdotal reports of resolution of severe pulmonary vascular disease in the remaining lung after single lung transplant. There are, however, some patients who maintain a high level of pulmonary vascular resistance and are refractory to vasodilator therapy despite what appear to be mild vascular changes on light microscopy (medial hypertrophy), P. For these patients, the prognosis may be not much better than those with unexplained pulmonary hypertension (22). A recent study of outcomes of patients with congenital heart disease (systemic-to-pulmonary shunt lesions) and pulmonary hypertension in the current treatment era demonstrated significantly decreased 20- year survival in patients with residual pulmonary vascular disease following defect closure (36%) relative to patients with Eisenmenger syndrome (87%) or those patients with an unrepaired systemic-to-pulmonary shunt without Eisenmenger syndrome (86%). While preoperative hemodynamics are unknown for the surgically repaired group, the late average age at operation may suggest advanced pulmonary vascular disease at the time of operation and inability of the right ventricle to adapt to the increased workload (23). Therapies for the patient with Eisenmenger syndrome have included chronic oxygen, anticoagulants, and palliative surgical procedures, including atrial septal defect creation and intravenous as well as, more recently, subcutaneous, inhaled, or oral prostacyclin analogs. In some cases, these measures have improved the quality of life and in others they have acted as a bridge to a heart–lung transplant or surgical correction along with lung transplant. More recent addition of phosphodiesterase inhibitors and endothelin receptor antagonists in this group of patients awaits the results of clinical trials, but is discussed later in this chapter, and in the subsequent chapter, with regard to patients with idiopathic pulmonary hypertension. Pathophysiology Based Upon Further Pathologic Assessments Recent immunohistochemical studies have been carried out in lung biopsy tissue from patients with congenital heart defects to elucidate mechanisms that are directly related to enhanced proliferation and migration of cells in the neointima with characteristics of smooth muscle cells. There is a progressive increase in the deposition of two matrix glycoproteins, tenascin and fibronectin, in the media and neointima (Fig. We previously related the increased expression of tenascin to vascular smooth muscle cells P. Fibronectin has been related to increased migration of smooth muscle-like cells in the context of neointimal formation. It is also proposed that endothelial cell proliferation and a form of angiogenesis is observed with plexiform lesions. The plexiform lesions in pulmonary hypertension associated with congenital heart disease appear to be derived from different clonal populations of endothelial cells compared with those observed in unexplained pulmonary hypertension where a single clone is usually found (25). Tenascin-C, proliferation and subendothelial fibronectin in progressive pulmonary vascular disease. Creation of large aortopulmonary shunts in dogs, particularly into a single pulmonary artery, resulted in more rapidly progressive pulmonary vascular changes. There are several other experimental models of high-flow congenital heart defects such as sheep or calves after an aortopulmonary lobar anastomosis.

The x-ray shows cardiomegaly with right atrial prominence purchase genuine cefadroxil, increased pulmonary vascular markings generic cefadroxil 250mg with visa, and prominent main pulmonary artery cheapest generic cefadroxil uk. D: Subcostal sagittal view of right atrial type of sinus venosus defect (asterisk) showing a large defect in the posterior right atrial wall. The enlarged right atrium, right ventricle, and pulmonary arteries also are seen on 2-D imaging. The volume- overloaded right ventricle causes diastolic flattening and paradoxical motion of the interventricular septum (Fig. Associated anomalies such as pulmonary stenosis, mitral valve prolapse, and anomalous pulmonary venous return also should be evaluated using 2-D imaging. M-mode imaging of the ventricles will show an enlarged right ventricle and paradoxical septal motion (Fig. This shunt usually is left-to- right, but in patients with elevated pulmonary artery pressure, a bidirectional shunt or a right-to-left shunt can be seen. Pulsed-wave Doppler shows interatrial shunting in late systole and early diastole. Since the pressure gradient across the atrial septum is minimal when these defects are nonrestrictive, low-velocity flow is noted using Doppler. However, a quantitative assessment of the pulmonary to systemic blood flow ratio ( Qp: Qs) also can be made. For this, the time velocity integrals obtained by tracing the pulsed-wave Doppler of pulmonary and aortic outflow are multiplied by the area of pulmonary and aortic valve, respectively. This has been shown to have a close correlation with the Qp: Qs measured invasively by oximetry during cardiac catheterization (32). Presence of right ventricular outflow tract obstruction, semilunar valve insufficiency, and patent ductus arteriosus limit the use of this method (33). A large left-to-right shunt may result in a flow-related peak gradient of as much as 30 mm Hg across the pulmonary valve. However, with higher gradients, one must suspect associated pulmonary valvular stenosis. Progressive tricuspid regurgitation resulting from tricuspid annular dilation and lack of coaptation of leaflets can be seen with significant right ventricular dilation. Doppler assessment for estimating pulmonary artery pressure can be performed by measuring the tricuspid and pulmonary regurgitant jets and applying the modified Bernoulli equation to calculate transvalve gradients and adding estimated right atrial pressure and right ventricular P. Development of pulmonary hypertension results in worsening of tricuspid and pulmonary regurgitation. The right ventricle becomes hypertrophied, and its systolic function starts deteriorating. B: Amplatzer septal occluder used to close the atrial septal defect (arrow) (Video 28. Due to the close proximity of the transducer to the cardiac structures, transesophageal imaging allows better spatial resolution and superior images of the atrial septum compared with transthoracic imaging (Fig. A left-to-right shunt is seen as a negative contrast washout into the right atrium, when the right atrium is opacified with contrast. A right-to-left shunt is detected by the presence of microbubbles in the left atrium and ventricle, and this effect can be augmented by performing a simultaneous Valsalva maneuver. It provides excellent 2- D and color-Doppler imaging of the interatrial septum and the surrounding structures. This technique has the advantage of eliminating the need for general anesthesia and additional personnel to perform transesophageal echocardiography. However, due to the large size of the sheath required to insert the catheter, its use in smaller children is limited (42). Angiography can be helpful in diagnosing associated lesions such as partial anomalous pulmonary venous return or mitral stenosis. During catheterization, a step-up in oxygen saturations in the right atrium will be noted in the presence of an atrial level left-to-right shunt. Qp:Qs can be calculated using the standard Fick equation or indicator dilution technique. In the absence of any other major cardiac anomalies, the presence of a small left-to-right shunt (Qp:Qs < 1. Direct measurement of intracardiac and pulmonary artery pressure can be performed during catheterization, and pulmonary vascular resistance can be calculated. In the presence of a large defect, there is minimal gradient between the two atria and there can be a flow-related gradient across the pulmonary valve as high as 30 mm Hg. In cases of pulmonary hypertension, acute response to pulmonary vasodilators such as nitric oxide and oxygen generally has been used to assess the reversibility and make decisions regarding closure. In cases where the symptoms are discordant with the clinical findings, it can be useful to document the exercise capacity. Exercise testing can be helpful in documenting oxygen saturations during exertion in patients with pulmonary hypertension, though maximal exercise is not recommended in the presence of severe pulmonary hypertension (52). Since the advent of echocardiography, it is possible to report data from serial echocardiographic evaluations estimating the change in the size of the defect and the rate of spontaneous closure (54,55,56). In general, most defects <5 mm that were recognized during infancy are likely to spontaneously close, while those larger than 8 to 10 mm are unlikely to do so. In seven asymptomatic patients, the defect size was 1 to 6 mm at a mean follow-up of 13. At a mean follow-up of about 14 months, spontaneous closure occurred in all the defects that were <3 mm at diagnosis, in 87% of defects that were 3 to 5 mm, in 80% of defects that were 5 to 8 mm, and in none of the defects that were ≥8 mm. Eventually, when there is reversal of the left-to-right shunt, these patients become progressively cyanotic and symptomatic. Acute response to vasodilators during cardiac catheterization is helpful to determine reversibility, though some cases may still fall into an indeterminate zone where it is difficult to differentiate between a reversible and an irreversible state. In rare cases when they are symptomatic, anticongestive therapy with diuretics may be indicated until closure is accomplished. In asymptomatic patients with a large shunt, elective closure between 2 and 5 years of age is recommended (62). However, early closure during infancy should be considered in those with compromised lungs since even a small amount of left-to-right shunt may not be well tolerated by them. This includes infants who are already predisposed to pulmonary hypertension such as those with chronic lung disease, diaphragmatic hernia or those who are ventilator-dependent for any other reasons (63). Even though most children with large defects may be asymptomatic, elective closure is recommended to prevent long-term complications such as atrial arrhythmias, paradoxical embolism, pulmonary hypertension, severe right ventricular dilation and dysfunction with overt symptoms of congestive heart failure, and hemodynamically significant mitral and tricuspid insufficiency. Closure of small defects without any right-sided cardiac enlargement is controversial. Routine follow-up of these patients during adulthood should include assessment for atrial arrhythmias and paradoxical embolic events and an echocardiogram every 2 to 3 years to evaluate right atrial and ventricular size and pressures (52). Use of autologous pericardial patch has eliminated the need to use prosthetic material, thereby theoretically, minimizing the risks of thromboembolism and endocarditis.

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